Exhaustive Cycle Exercise Induces P-Selectin Expression, Coagulation, and Fibrinolysis Activation in Ultraendurance Athletes

Möckel, Martin; Ulrich, Natalie-Viviane; Röcker, L.; Ruf, Andreas; Klefisch, Frank; Patscheke, Heinrich; Eichstädt, H.; Störk, T.; Frei, Ulrich

doi:10.1016/s0049-3848(99)00008-0

Cited by 19 publications

(12 citation statements)

References 24 publications

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“…These results are in keeping with the findings of Mockel et al 12 in younger athletes; however, they contradict those of Kestin et al 8 who found marked platelet activation only in a sedentary population. The changes are seen to persist in the recovery period from strenuous exercise with shortening of the APTT and increasing antifibrinogen antibody expression.…”

Section: Discussionsupporting

confidence: 88%

“…Platelet activation has been reported with exercise in a sedentary population with no activation seen in a trained population 8. This conflicts with the study of Mockel et al ,12 showing that in a young population of ultra endurance athletes, exhaustive cycling causes platelet activation demonstrated by the expression of P-selectin, with the greatest effects seen after anaerobic exercise. Wang et al 13 had previously reported that platelet activation may be related to exercise intensity, with activation seen with strenuous exercise and no change with moderate exercise.…”

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confidence: 86%

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The effects of acute dynamic exercise on haemostasis in first class Scottish football referees

et al. 2008

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This study suggests that in an older athletic population, physical fitness does not protect against the prothrombotic effects of exercise. These data suggest that during a football match when referees achieve approximately 80% of peak VO2 (23) they may be at risk of significant platelet activation. Prophylactic platelet inhibition should be considered in this group after appropriate screening and risk stratification.

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Section: Discussionsupporting

confidence: 88%

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confidence: 86%

The effects of acute dynamic exercise on haemostasis in first class Scottish football referees

et al. 2008

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“…1,2 Yet the general acceptance of this suggestion is problematic as physical activity can be enganged in differently regarding intensity and/or the duration of exercise. 4,5 But the studies of Mo¨ckel et al did not include a control group. For example, in one study, Kestin et al could show that the reaction of the platelets depended on the physical performance of the test subjects.…”

Section: Introductionmentioning

confidence: 99%

Short-term exercise and platelet activity, sensitivity to agonist, and platelet-leukocyte conjugate formation

et al. 2003

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Strenuous exercise may be partially responsible for cardio-vascular events. The aim was to investigate the platelet activity, reactivity and different platelet-leukocyte-conjugate formation following maximal short-term exercises. Fifteen healthy non-smokers underwent three isokinetic maximal tests on a SRM cycle ergometry system with durations of 15, 45 and 90 s. Blood samples were taken after a 30-min rest, immediately before and after exercise, and 15 min and 1 h after completion of exercise. Platelets were detected flow-cytometrically by CD41, and activated platelets by CD62P. In addition, stimulation of the platelets in vitro with 7.5 microM TRAP-6 was initiated. For testing platelet-leukocyte-conjugates, antibodies against CD45, CD14 and CD41 were used. After the exercise tests the percent of non-stimulated CD62P-positive platelets (%PC) was unchanged. In contrast, an increase in %PC (CD62P) TRAP-6 stimulated (15-s test: 37.2+/-10.3 to 46.2+/-12.3%, P < 0.05; 90-s test: 40.6+/-9.5 to 51.7+/-10.2%, P < 0.01) and in platelet-granulocyte, platelet-lymphocyte, and platelet-monocyte conjugate formation 15 min after exercise (45- and 90-s test; P < 0.05) were observed in comparison with the changes on the control day. The changes nearly reversed 1 h after exercise. Maximal short-term exercise only leads to a moderate increase of platelet reactivity and to an increase in the different platelet-leukocyte conjugates. The implications of the changes in platelet-leukocyte conjugate formation should be investigated in future studies.

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“…Platelet adhesion, fibrinogen binding to platelet fibrinogen receptors and intracellular calcium mobilization are also enhanced after exercise [148]. Finally, physical exercise increases the binding of [3H]-ketanserin to the serotonin-2A (5-HT2A) receptors on platelets [149], oxidative stress [150] and surface expression of Pselectin [151]. It was shown that exercise training affects the prostaglandin system via enhanced prostacyclin consumption and inhibition of thromboxane release [152,153].…”

Section: Platelet Markersmentioning

confidence: 99%

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

Serebruany¹,

Davis

Meister

et al. 2001

Heart Drug

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Knowledge of the pathogenesis of congestive heart failure (CHF) has improved greatly in recent years. Nevertheless, this disease still causes high morbidity and mortality in the Western world. In particular, there have been many advancements in our understanding, treatment and prophylaxis of CHF in recent years, yet the incidence of this disease continues to rise. Due to the staggering numbers of patients afflicted, CHF is becoming the most expensive burden on the health care system. The relationship between the deterioration of cardiac function and ongoing ischemic events has not been fully investigated and could conceivably be both monitored and modulated via various biomarkers. Recent data also indicate that heart failure is associated with altered hemostasis, i.e. a prothrombotic state which can lead to complications arising from occlusive and/or thromboembolic phenomena. Although the incidence of overt and clinically apparent thrombotic events is low, it is possible that subclinical events contribute to the increasing morbidity and mortality from this disease. These subclinical events may include silent ischemic events or microinfarcts which are being recognized as contributing to the progression of heart failure. As far as nonpharmacologic approaches to heart failure are concerned, the use of uniform exercise training regimens in heart failure is still a very controversial topic. Before more definitive recommendations can be made regarding the justification of such procedures, further large-scale studies investigating the effects of physical exercise on the development and progression of heart failure are needed. Furthermore, these studies must have sufficient statistical power to detect effects on clinical outcomes, specifically mortality. The purpose of this review article is to bridge the gap between biomarkers, exercise training and heart failure by discussing our current knowledge of different markers of platelet activation, thrombin generation, inflammation, endothelial dysfunction and myocardial necrosis in CHF patients undertaking physical exercise.

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Exhaustive Cycle Exercise Induces P-Selectin Expression, Coagulation, and Fibrinolysis Activation in Ultraendurance Athletes

Cited by 19 publications

References 24 publications

The effects of acute dynamic exercise on haemostasis in first class Scottish football referees

The effects of acute dynamic exercise on haemostasis in first class Scottish football referees

Short-term exercise and platelet activity, sensitivity to agonist, and platelet-leukocyte conjugate formation

Biomarkers and Exercise Training: A Possible Missing Link between Physical Activity and Mortality Benefit in Patients with Heart Failure

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